ArticleBiomechanics and modeling in mechanobiology2013
Calcific nodule morphogenesis by heart valve interstitial cells is strain dependent.
Article in Biomechanics and modeling in mechanobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 103 citations in OpenAlex.
- From biomechanical mechanisms to clinical reasoning: Deciphering mechanobiological drivers of aortic valve calcification for precision therapy.Mechanobiology in medicine · 2026Review
- Capturing Multiscale Dynamics of Aortic Valve Calcification with a Coupled Fluid-Structure and Systems Biology Model.ACS omega · 2026Article
- Reversion of aortic valve cells calcification by activation of Notch signalling via histone acetylation induction.Signal transduction and targeted therapy · 2025Article
- Emerging mechanomedicines informed by mechanotransduction along the integrin-cytoskeleton-nucleus axis.APL bioengineering · 2025Review
- Insights into preclinical models of calcific aortic valve disease and their translational potential.Frontiers in cardiovascular medicine · 2025Review
- Diabetes and calcific aortic valve disease: implications of glucose-lowering medication as potential therapy.Frontiers in pharmacology · 2025Review
- Unraveling the Mechanisms of Valvular Heart Disease to Identify Medical Therapy Targets: A Scientific Statement From the American Heart Association.Circulation · 2024Review
- Biomechanical Remodeling of Aortic Valve Interstitial Cells During Calcified Lesion Formation In Vitro.Annals of biomedical engineering · 2024Article
- Analysis of fibrocalcific aortic valve stenosis: computational pre-and-post TAVR haemodynamics behaviours.Royal Society open science · 2024Article
- Computational study of transcatheter aortic valve replacement based on patient-specific models-rapid surgical planning for self-expanding valves.Frontiers in physiology · 2024Article
- The Role of Apoptosis and Oxidative Stress in a Cell Spheroid Model of Calcific Aortic Valve Disease.Cells · 2023Article
- Predicting key gene related to immune infiltration and myofibroblast-like valve interstitial cells in patients with calcified aortic valve disease based on bioinformatics analysis.Journal of thoracic disease · 2023Article
- Multicellular aligned bands disrupt global collective cell behavior.Acta biomaterialia · 2023Article
- A Doppler-exclusive non-invasive computational diagnostic framework for personalized transcatheter aortic valve replacement.Scientific reports · 2023Article
- Cardiovascular Calcification Heterogeneity in Chronic Kidney Disease.Circulation research · 2023Review
- Sclerostin ablation prevents aortic valve stenosis in mice.American journal of physiology. Heart and circulatory physiology · 2022Article
- Progressive Calcification in Bicuspid Valves: A Coupled Hemodynamics and Multiscale Structural Computations.Annals of biomedical engineering · 2021Article
- Predictors of calcification distribution in severe tricuspid aortic valve stenosis.The international journal of cardiovascular imaging · 2021Article
- Inflammatory and Biomechanical Drivers of Endothelial-Interstitial Interactions in Calcific Aortic Valve Disease.Circulation research · 2021Review
- Degeneration of Aortic Valves in a Bioreactor System with Pulsatile Flow.Biomedicines · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Calcific aortic valve disease (CAVD) results in impaired function through the inability of valves to fully open and close, but the causes of this pathology are unknown. Stiffening of the aorta is associated with CAVD and results in exposing the aortic valves to greater mechanical strain. Transforming growth factor β1 (TGF-β1) is enriched in diseased valves and has been shown to combine with strain to synergistically alter aortic valve interstitial cell (AVIC) phenotypes. Therefore, we investigated the role of strain and TGF-β1 on the calcification of AVICs. Following TGF-β1 pretreatment, strain induced intact monolayers to aggregate and calcify. Using a wound assay, we confirmed that TGF-β1 increases tension in the monolayer in parallel with α-smooth muscle actin (αSMA) expression. Continual exposure to strain accelerates aggregates to calcify into mature nodules that contain a necrotic core surrounded by an apoptotic ring. This phenotype appears to be mediated by strain inhibition of AVIC migration after the initial formation of aggregates. To better interpret the extent to which externally applied strain physically impacts this process, we modified the classical Lamé solution, derived using principles from linear elasticity, to reveal strain magnification as a novel feature occurring in a mechanical environment that supports nodule formation. These results indicate that strain can impact multiple points of nodule formation: by modifying tension in the monolayer, remodeling cell contacts, migration, apoptosis, and mineralization. Therefore, strain-induced nodule formation provides new directions for developing strategies to address CAVD.
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